ATF2 on the double – activating transcription factor and DNA damage response protein

Bhoumik, Anindita; López-Bergami, Pablo; Ronai, Ze’ev A.

doi:10.1111/j.1600-0749.2007.00414.x

Cited by 89 publications

(82 citation statements)

References 91 publications

(100 reference statements)

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“…ATF2 has multiple roles in a cell; in the nucleus it can impact transcription (via heterodimerization with c-Fos or c-Jun) and be involved in chromatin remodeling and DNA repair; in the cytoplasm ATF2 interacts with voltage-dependent ion channels, affecting mitochondria permeability. 24,25 Other studies have highlighted JNK-mediated DNA damage, phosphorylation of Bcl-2 and Bim, or increased expression of Bax, Bak, Puma or Noxa in response to long exposures (24 h) of microtubule disrupting agents in solid tumors. [26][27][28] However, with the exception of increased Noxa, we did not observe these other biomarkers in leukemia (data not shown), and acute Noxa induction does not appear to rely solely on JNK signaling.…”

Section: Discussionmentioning

confidence: 99%

Rapid induction of apoptosis in chronic lymphocytic leukemia cells by the microtubule disrupting agent BNC105

Bates

Feris

Danilov

et al. 2016

Cancer Biology & Therapy

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Microtubule targeting agents, such as vinblastine, are usually thought to arrest cells in mitosis and subsequently induce apoptosis. However, they can also cause rapid induction of apoptosis in a cell-cycle phase independent manner. BNC105 is a novel vascular and microtubule disrupting drug that also induces apoptosis rapidly but with markedly increased potency compared to vinca alkaloids and combretastatin A4. BNC105 binds to the colchicine-binding site on tubulin resulting in activation of c-Jun N-terminal kinase (JNK), phosphorylation of ATF2, and induction of ATF3 and Noxa leading to acute apoptosis in chronic lymphocytic leukemia (CLL) cells. Apoptosis induced by BNC105 is dependent upon both JNK activation and Noxa induction. Normal leukocytes and one CLL sample also exhibited JNK activation but not Noxa induction and were resistant to BNC105. This study emphasizes the importance of Noxa and JNK for induction of apoptosis in CLL cells by microtubule targeting drugs, and highlights the potential of BNC105 as a potent therapeutic to treat haematopoietic malignancies.

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Section: Discussionmentioning

confidence: 99%

Rapid induction of apoptosis in chronic lymphocytic leukemia cells by the microtubule disrupting agent BNC105

Bates

Feris

Danilov

et al. 2016

Cancer Biology & Therapy

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“…However, the most surprising conclusion from the knockout mouse work is that ASCIZ has a major function in vivo as a crucial, likely transcriptional, regulator of embryonic development, particularly of the respiratory system. In this sense, ASCIZ joins a growing list of proteins such as Sp1, 13,14 PTIP 15 and ATF 16 with important developmental roles as transcriptional regulators that are separate from their scaffold functions as ATM substrates in the DNA damage response. A better understanding of the molecular mechanisms involved in the two diverse functions of ASCIZ using an expanded range of conditional deletions and by the generation of specific separation-of-function alleles, might thus also provide useful insights into the regulation of these other proteins with dual functions in transcription and the DNA damage response.…”

Section: Severe Organ Development Defects Including Complete Absence mentioning

confidence: 99%

A breathtaking phenotype: Unexpected roles of the DNA base damage response protein ASCIZ as a key regulator of early lung development

Heierhorst

Smyth²,

Jurado

2011

Cell Cycle

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The ATM substrate Chk2-interacting Zn 2+ -finger protein (ASCIZ, also known as ATMIN and ZNF822) has previously been reported to be important for the repair of methylating and oxidative DNA damage, and it has also been proposed to regulate the stability and DNA damage-independent activation of the ATM kinase. While the role of the protein in the regulation of ATM remains controversial, two recent ASCIZ mouse knockout papers confirm its role in the DNA base damage response, including oxidative stress resistance in vivo. Similar to other DNA base damage repair proteins, ASCIZ is essential for embryonic development, with lethality of Asciz-null embryos around day E16.5 post conception. Unexpectedly, absence of ASCIZ also leads to severe organ development defects, most notably, complete absence of lungs similar to mutants in Wnt2-2b/b-catenin and FGF10/ FGFR2b signaling pathways. Together with evidence that ASCIZ can activate transcription in vitro, the phenotype indicates that ASCIZ has dual functions as an efficiency factor for DNA base damage repair as well as a key transcriptional regulator of early lung development.

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“…Among others, genes targeted by amATF-2 regulate transcription factors and proteins engaged in stress and DNA damage response (Bhoumik et al 2007). (3) amDHAP-AT: Dihydroxy acetone phosphate acyl transferase is involved in lipid metabolism, facilitating the production of triacylglycerides (TAG).…”

Section: Introductionmentioning

confidence: 99%

RNA interference in honeybees: off-target effects caused by dsRNA

Jarosch

Moritz

2011

Apidologie

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RNA interference involves the targeted knockdown of mRNA triggered by complementary dsRNA molecules applied to an experimental organism. Although this technique has been successfully used in honeybees (Apis mellifera), it remains unclear whether the application of dsRNA leads to unintended expression knockdown in unspecific, non-targeted genes. Therefore, we studied the gene expression of four non-target genes coding for proteins that are involved in different physiological processes after treatment with three dsRNAs in two abdominal tissues. We found unspecific gene downregulation depending on both the dsRNA used and the different tissues. Hence, RNAi experiments in the honeybee require rigid controls and carefully selected dsRNA sequences to avoid misinterpretation of RNAi-derived phenotypes.

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ATF2 on the double – activating transcription factor and DNA damage response protein

Cited by 89 publications

References 91 publications

Rapid induction of apoptosis in chronic lymphocytic leukemia cells by the microtubule disrupting agent BNC105

Rapid induction of apoptosis in chronic lymphocytic leukemia cells by the microtubule disrupting agent BNC105

A breathtaking phenotype: Unexpected roles of the DNA base damage response protein ASCIZ as a key regulator of early lung development

RNA interference in honeybees: off-target effects caused by dsRNA

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